1. Anaerobes: structure
    • Require less than 10% O2
    • Lack catalase or superoxide dismutase
    • Clostridia: spore forming, C Perfringens, C Botulinum and C Tetani, C difficile
    • Propionobacteria: commensal skin flora
    • Bacteriodes: Gram negative, Beta lactamase production, B Fragilis
  2. Anaerobes: Epidemiology
    • Colozine oxygen deficient tissues
    • Skin, gingival surfaces, intestinal lumen
    • Usually autoinfections
  3. Anaerobes: pathogenesis
    • Usually displaced from biological niche
    • trauma, disease, aspiration
    • impaired blood supply increases risk
    • usually commensal adjacent to site of infection
    • Some distance from site of infection and commensal site may be observed (i.e. aspiration of oral flora -> pneumonia, brain abcess)
    • Additional virulence factors needed (i.e. ability to withstand O2)
  4. Anaerobes: manifestations
    • Localized abcesses in cranium, thorax, peritoneum, live, and GU tract
    • Nerve toxins as well
    • Diagnosis: high quality specimen from site of infection, gram stain, isolation in anaerobic jar
    • Tx: Drainage of purulent material
  5. C. Perfreingens
    • Large gram positive rod, forms spores, produces gas in necrotic tissues, alpha toxin hydrolizes lecithin and sphingomyelin
    • Epi: Gas gangrene develops in severe traumatic open lesions with muscle necrosis
    • Pathogenesis: low oxidation reduction potential -> spores germinate -> alpha-toxin -> more tissue necrosis -> shock
    • Food poisoning: spores survive cooking and are ingested
    • Gas Gangrene: fermentation of muscle carbs -> gas (crepitation); excision of all devitalized tissue; massive doses of penicillin; surgical debridement most important
    • Food poisoning: 8-24 hours -> nasua, abdominal pain, diarrhea; meat dishes
  6. C. Botulinum
    • Environmental bacterial, gram positive rod, spore forming, toxins are heat labile and resistant to enzymes, toxins work at NM junction and black Ach release
    • Epi/Patho: ingestion of home canned beans not heated sufficiently; organism multiplies in can and elaborates toxin
    • Botulism: 18-96 hours; ocular, pharyngeal, laryngeal muscle paralysis which may progress to massive voluntary muscle paralysis
    • infant botulism: honey; multiplesin colon; constipation, poor muscle tone, lethargy
    • tx: supportive measures; horse anti-toxin
  7. C Tetani
    • Gram positive, spore forming, environmental, toxin = tetanospasmin, heat labile, antigenic, and neutralized by intestinal proteases
    • epi: introduced into wounds by contaminated soil, wounds usually small
    • Patho: low redox area; germination of spores, txoin made at site of infection and reaches CNS by ascending motor nerves; acts on anterior horn cells -> unopposed neuron firing; muscle spasms
    • Tetanus: 4 days -weeks; masseter muscles first affected (lockjaw), generalized convulsions
    • Tx: tetanus anti-toxin
    • Prevention: DPaT
  8. C. Diff
    • Commensal organism, toxin-A=enterotoxin ->fluid secretion, hemorrhagic necrosis; toxin B=cytotoxin
    • Pathogenesis: alteration of colonic flora with antibiotics; overgrowth of c. diff, psuedomembrane developes
    • PMC: diarrhea (mild and watery or bloody and cramping with fever)
    • Diagnosis: Toxins detected in stool
    • Treatment: Vancomycin (poor adsorption)
  9. B. Fragilis
    • Commensal intestinal flora, deep pain and tenderness below diaphragm, gram negative rod, tolerant of O2, polysaccharide capsule
    • Pathogenesis: Major organism of abdominal cavity infections; capsule prevents phagocytosis, stimulates abcess formation; fever may be present
    • Tx: usually resistant to beta lactams; clindamycin
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